In the next year of this project investigation will continue regarding the role of insulin in the control of hepatic ketogenesis and glycogen synthesis. Efforts will be made to explain the paradox that insulin given in vivo causes glycogen synthesis and reverses ketogenesis while the hormone added to the isolated perfused liver and isolated hepatocytes does not. Both in vitro preparations can be stimulated to given maximal rates of glycogen formation by the inclusion of a gluconeogenetic precursor and an amino acid such as glutamine. The possibility that a factor released from the pancreatic islets or intestinal mucosa is necessary for glycogen formation will be explored.